Human Respiratory System
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Mechanism of Breathing
•
Ventilation (breathing) is the term for the movement of air
to (inspiration) and from (expiration) the alveolus.
•
Exhalation / expiration is followed by inhalation /
inspiration. They are brought about by Nervous System
and respiratory muscles.
•
Medulla generate impulses to respiratory muscles.
Respiration is the sequence of events that results in
gas exchange between the environment and the
body cells.
 External Respiration
 Internal Respiration
A- External respiration: Involves gas exchange (O2
and CO2) with the external environment: exchange
between lungs and blood.
B. Involves gas exchange between the blood and
tissues.
Internal respiration or Cellular Respiration: is
process of ATP production by cells.
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 External
Respiration
Respiratory
Systems
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1. Gas exchange
between the air in
the alveoli and the
blood in the
pulmonary
capillaries is
achieved by
simple diffusion.
2. The blood coming
into pulmonary
capillaries is rich
in CO2 and poor
in oxygen.
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3. CO2 diffuses from higher concentration in the blood across the
walls of alveolar capillaries to lower concentration in the air in the
alveoli.
4. The blood coming into pulmonary capillaries is oxygen poor and
the alveolar air is oxygen-rich.
5. Oxygen diffuses from higher concentration in alveoli across the
walls of the alveolar capillaries to the lower concentration in the
blood.
6. The end result is that alveoli contain high concentrations of CO2
and low concentration of O2 this situation changes by exhalation.
Exhalation is followed by inhalation of atmospheric air which contains
little CO2, and high O2 levels.
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Diffusion is very rapid
due to :
Very large surface area of
the lungs: Human lungs
have at least 50 times the
skin’s surface area.
Very small diffusion
distance between the air
in the alveoli and the
blood in the pulmonary
capillaries.
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Air–blood barrier
contains 2 types of cells:
A-capillary endothelial
cell
B-alveolar cell: alveolar
cells are two types: type
I type II and
macrophages.
•
The human respiratory system includes conducting region and
respiratory region.
•
Conducting region is everything that conducts air to and from the
lungs; the lungs lie deep within the thoracic cavity for protection
against drying.
•
Air moves into the nose, crosses the pharynx, flows through the
glottis (an opening into the larynx or voice box) to the trachea,
bronchi, bronchioles, and finally the alveoli, where gas exchange
occurs.
•
This process filters debris, warms the air, and adds moisture
(humidification).
•
When the air reaches the lungs, it is at body temperature and is
saturated with water.
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
The larynx, or voice box, is located at the entrance of the trachea.
The larynx houses the vocal folds (vocal cords). The vocal folds
are situated just below where the tract of the pharynx splits into
the trachea and the esophagus. As air passes across vocal cords
they vibrate creating sounds.

When food is being swallowed, the glottis is closed by the
epiglottis.

Beyond the larynx the trachea divides into two main branches,
the right and left bronchi, which enter the right and lift lung
respectively.
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Trachea and bronchi are
lined with cilia that
beat upward carrying
mucus, dust, and any
food particles that went
the wrong route.
The trachea walls are
reinforced with
C-shaped rings of
cartilage.
Within the lungs, each
bronchus branches
into numerous
bronchioles that
conduct air to alveoli.
Alveoli are microscopic air
sacs.
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Respiratory
Systems
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Respiratory Zone:
Function: Gas exchange.
Structures are :
1. Respiratory
bronchioles
2. Alveolar duct
3. Alveoli.
Alveoli are microscopic
air sacs.
Histology of Alveolar Wall
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1. Type I pneumocyte (P I cells): Covers 95% of alveolar
wall surface area. They are flat cells (too thin to have
organelles), which makes them very suitable for gas
exchange.
2. Type II pneumocyte (P II cells): Rounded cells, cover 3%
of alveolar surface. These are plump / cuboidal with surface
microvilli. They produce the surfactant which reduces
water surface tension.
3. Alveolar macrophages constitute a small percentage, but
represent the main cellular host defense mechanism in the
alveolar space. They are part of the mononuclear phagocyte
system and are derived primarily from blood Monocytes.
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Each alveolus
is surrounded
by a network of
pulmonary
capillary
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In late fetal life: Type II cells start to develop at about 24
weeks of gestation, secreting small amounts of surfactant.
However, adequate amounts of surfactant are not secreted
until about 35 weeks of gestation - this is the main reason for
increased incidence rates of infant respiratory distress
syndrome (IRDS).
P-II cells secrete a phospholipid (like phosphatidyl
choline, phosphatidyl glycerol,…) that lowers surface
tension; called surfactant (surface active agent), that
prevents alveoli from collapsing during expiration.
IRDS: Premature babies are sometimes born with lungs
with insufficient surfactant, and their alveoli collapse.
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Infant respiratory
distress syndrome:
also called Hyaline
membrane
syndrome.
Without surfactant
the surface tension
causes the alveolus
to collapse after
each breath rather
than remain inflated.
Each breath
therefore is difficult.
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Lungs are covered by
double layer membrane
called PLEURA,
Parietal pleura that is
attached to the bony
thorax
and
Visceral pleura that is
attached to the lung
surface.
In between the parietal
and visceral pleura exists
a cavity containing a thin
fluid named pleural
cavity.
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Air movement into and out of the lungs occurs due to pressure
differences induced by changes in lung volumes.
Air flows from higher to lower pressure areas. It is directly
proportional to pressure difference.
When intrapulmonary pressure is lower than atmospheric
pressure it is called subatmospheric pressure OR negative
pressure.
Humans respire using a tidal ventilation mechanism; negative
pressure in the lungs allows for air flow during inspiration.
During inhalation, lowering the diaphragm and raising the
ribs forms a negative pressure by increasing the volume of
the thoracic cavity; the air–under greater outside pressure–
flows into the lung.
Boyle's law
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Pressure of a gas is inversely proportional to its
volume (at fixed temp.).
During (inspiration)
Lung volume  intrapulmonary pressure   air
goes in.
Create negative pressure in the thoracic cavity and
lungs, and then air flows into the lungs.
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Mechanics of Breathing (pulmonary ventilation)
Phases of Breathing:
1- inspiration (inhalation)
2-expiration (exhalation)
They are due to increasing and decreasing thorax and lungs volumes.
For inspiration to occur, lungs must be able to expand/stretch
(compliance); for expiration to occur, lungs must get smaller
(elasticity). The tendency to get smaller is also aided by surfactant.
Increasing volumes by muscle contractions that lower the
diaphragm and raise the ribs.
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Inspiration Versus Expiration
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Mechanics of inspiration
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Contraction of diaphragm & external intercostal muscles  lung
volume   intrapulmonary pressure  forces air into lungs.
• Inhalation
• Active process
 During quiet breathing contraction of diaphragm and external
intercostals expands thoracic cavity
 Decreases pressure (Boyle’s law – volume inversely related to
pressure)
 Air flows down pressure gradient.
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Forced / deep inspiration
Contraction of accessory
respiratory muscles: these are
1-Scalene
2-Pectoralis minor
3-Sternocleidomastiod
Which will increase the
volume anteriorly and
posteriorly.
Mechanics of expiration
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Quiet expiration totally passive mechanism lungs recoil (elasticity) to
their original size due to muscles relaxation.
Diaphragm relaxation &external interalcostal muscles relaxation
lung volume   intrapulmonary pressure  forces air out of lungs.
• Exhalation during quiet breathing is passive process due to: Recoil of
elastic fibres & inward pull of surface tension of alveolar fluid
• Forced expiration: results from:
1-The contraction of internal intercostal muscles depresses the rib cage.
2- Abdominal muscles contract putting pressure on the internal organs
which push against the diaphragm moving it up which decrease the
volume of thorax.
Pulmonary Function Test.
Pulmonary function may be assessed clinically by
means of a technique known as spirometry, the
record of the breathing is called a spirogram.
It records:
1- lung volume
2- lung capacity
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Lung Volumes.
1. Tidal volume (TV; 500 ml): volume of gas inspired/expired of
restful breathing.
2. Inspiratory reserve volume (IRV; 3000 ml): maximum volume
that can be inspired during forced breathing other than tidal
volume.
3. Expiratory reserve volume (ERV; 1300 ml): maximum volume
of gas that can be expired during forced breathing other than
tidal volume.
4. Residual volume (RV; 1200 ml): volume of gas remaining in the
lungs after vital capacity (VC) expiration.
Lung Capacities: sum of two or more
lung volumes.
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7. Vital capacity (VC; 4700 ml): maximum air that can be expired after a
maximum inspiration.
8. Forced Expiratory volume (FEV): amount of gas that can be expired
forcedly in 1s, 2s, 3s.
Gas Exchange in the Lungs
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At sea level, one atmosphere = 760 mmHg (or 760 torr).
760 mmHg was measured by Barometer.
Atmospheric pressure is made of a mixture of gases so its pressure is
equal to the sum of the pressures exerted by each gas.
Dalton's law: In a mixture of gases, each gas exerts pressure (partial
pressure; P) in proportion to its percentage in the total mixture.
Since O2 percentage in atmosphere is 21% then
PO2= 760 × 21/100= 160 mmHg.
At High altitudes: total atmospheric pressure is low (PO2 is
low)
Partial Pressures of Gases in Blood, Lungs &
Tissues
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Alveoli air PO2 = 105 mmHg (only 60 mmHg O2 can
saturate Hb) and PCO2 = 40 mmHg.
Arterial blood PO2 = 100 mmHg; PCO2 = 40 mmHg.
Peripheral tissue PO2 = 40 mmHg; PCO2 = 46 mmHg.
Venous blood PO2 = 40 mmHg; PCO2 = 45 mmHg.
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Regulation of respiration
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1. Neural regulation
2. Chemical regulation
•
Nervous regulation
There are respiratory centers in the
 Medulla oblangata----rhythmicity center that controls
automatic breathing.
 Pons----- pneumotaxic and apneustic centers (fine tuning of
breathing).
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Medulla oblangata
The inspiration center automatically generates impulses in rhythmatic
spurts ‫ رشات‬.
These impulses travel along nerves to respiratory muscles to stimulate
their contraction. The result is inhalation.
As lung inflate baroreceptors in the lung tissue detect this stretching, and
generate sensory impulses to medulla. These impulses depress the
inspiration center .
This is named Hering–Breuer inflation reflex.
As inspiration center is depressed the result is decrease in impulse to
respiratory muscles which relax to bring about exhalation.
Then inspiration center become active again in another cycle.
When the is more forceful exhalation as during exercise, the inspiration
center activates the expiration center, which generate impulses to
internal intercostal muscles and abdominal muscles.
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Respiratory
Systems
 Pons----- pneumotaxic and apneustic centers (fine tuning of
breathing).
Apneustic center promotes inspiration.
Pneumotaxic center inhibits inspiration .
These centers receive impulses from the cerebral cortex,
hypothalamus, spinal cord, periphery and from stretch and
compression receptors in the lung.
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Factors that influence respiration
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Respiratory
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Regulation of respiration cont.
2. Chemical regulation
There are 2 groups of chemoreceptors that monitor changes in blood
PCO2, pH, and PO2:
1.
Central chemoreceptors in medulla oblongata
2.
Peripheral chemoreceptors in the aorta and carotid arteries.
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Systems
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chemoreceptors
Peripheral chemoreceptors
in the aorta and carotid arteries
Central chemoreceptors
located in medulla oblongata
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Peripheral chemoreceptors
include: aortic bodies, located
around aortic arch (send
sensory information to
medulla in the vagus nerve),
and carotid bodies (send
sensory signals via
glossopharyngeal nerve; IX)
located at the point where
each common carotid artery
branches into internal and
external carotid arteries .
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Systems
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Peripheral chemoreceptors
Chemoreceptor input to the brain stem modifies the rate and depth of
breathing so that arterial PCO2, pH & PO2 remain relatively constant
Peripheral
Chemoreceptor
Respiratory
Systems
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1-Hypoventilation  PCO2 &  pH (due to formation of
carbonic acid, which splits releasing H+). However, blood
O2 content decreases much more slowly because of the
large “reservoir” of O2 attached to hemoglobin (Hb).
CO2 + H2O → H2CO3 → H+ + HCO3
Hyperventilation  PCO2 &  pH, but does not
significantly increase O2 content, as Hb in arterial blood is
97% saturated with O2 during normal ventilation.
Thus, Aortic & carotid bodies are not stimulated directly by
blood CO2, but are stimulated by a rise in [H+] of arterial
blood, which occurs when blood CO2 (and thus H2CO3), is
raised.
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Medullary
chemoreceptors
Arterial PCO2   blood H+, however, H+ cannot
cross blood-brain barrier (cannot influence medullary
chemoreceptors), but CO2 can and through the
formation of H2CO3, lowers cerebrospinal fluid pH.
Medullary chemoreceptor response requires few
minutes before it gets into action. The immediate
increase in ventilation that occurs when PCO2 rises
is due to peripheral chemoreceptors stimulation.
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• Hypercapnia (increase of CO2 in arterial blood).
•  PCO2 &  pH (due to formation of carbonic acid, which
splits releasing H+).
• Blood and other body fluids are more acidic, medulla
respond by increasing ventilation.
• Hypercapnia normally triggers a reflex which increases
breathing and access to oxygen, such as arousal and turning
the head during sleep. A failure of this reflex can be fatal, as
in sudden infant death syndrome.
• hypercapnia can be accompanied by respiratory acidosis.
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Respiratory
acidosis –
occurs when
the rate or
efficiency of
respiration
decreases.
• Respiratory acidosis is a medical condition in
which decreased ventilation (hypoventilation) causes
increased blood carbon dioxide concentration and
decreased pH.
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Systems
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Hypocapnia
• Is a isiiis stateof reduced carbon dioxide in the arterial blood.
Hypocapnia usually results from deep or rapid breathing, known as
hyperventilation.
• hypocapnia causes cerebral vasoconstriction, leading to cerebral
hypoxia and this can cause transient dizziness, visual disturbances, and
anxiety. A low partial pressure of carbon dioxide in the blood also
causes alkalosis, leading to lowered plasma calcium ions and increased
nerve and muscle excitability. This explains the other common
symptoms of hyperventilation, muscle cramps and tetany in the
extremities, especially hands and feet.
• Because the brain stem regulates breathing by monitoring the level of
blood CO2, hypocapnia can suppress breathing to the point of blackout
from cerebral hypoxia.
• Respiratory alkalosis – occurs when the rate of respiration increases.
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Effects of Blood PO2 on Ventilation
The O2 content of the blood decreases much more slowly
because of the large reservoir of O2 attached to Hb.
So blood PO2 has little effect on breathing.
(low PO2  chemoreceptor sensitivity to PCO2 changes).
PO2 of arterial blood must fall from 100 mmHg to 50 mmHg
before ventilation is stimulated.
This stimulation is due to a direct PO2 effect on carotid
bodies. Since this degree of hypoxemia does not occur at sea
level, PO2 does not normally exert direct effect on breathing
because of the large reservoir of attached to Hb.
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Gas Exchange and Transport
1. Gas exchange between the air in the alveoli and the blood in
the pulmonary capillaries is primarily by diffusion.
2. Atmospheric air contains little CO2, but blood flowing in
the pulmonary capillaries has a higher concentration of CO2.
3. CO2 diffuses from higher concentration in the blood across
the walls of alveolar capillaries to lower concentration in the
air in the alveoli.
4. The blood coming into pulmonary capillaries is oxygen
poor and the alveolar air is oxygen-rich.
5. Oxygen diffuses from higher concentration in alveoli across
the walls of the alveolar capillaries to the lower
concentration in the blood.
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Hemoglobin (Hb) & O2 Transport
In each 100 mL of
oxygenated blood:
1.5% of O2 is dissolved in
plasma
98.5% is bound to Hb;
oxyhemoglobin (Hb-O2).
Hb consists of 4 polypeptides; 2 -chains & 2 -chains. Each chain
contains a heme group with Fe2+ (ferrous iron). The iron atom of a
heme group loosely binds with an O2 molecule.
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3 Types of Hemoglobin
1- oxyhemoglobin
2-Methemoglobin (met-Hb) : Oxidized Hb has Fe++ in
the oxidized (Fe3+/ferric) state. Met-Hb thus lacks the
e- it needs to form a bond with O2 and cannot
participate in O2 transport. Blood normally contains
only a small amount of met-Hb, but certain drugs can
increase this amount.
3- Carboxyhemoglobin: the reduced heme is combined
with CO instead of O2. Since the bond with CO is
210 times stronger than the bond with O2, CO
remains attached to Hb.
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Oxygen-binding ability of hemoglobin
a. The percentage of oxygen-binding sites of
hemoglobin carrying O2 varies with partial pressure
of O2 in the immediate environment.
b. At a normal partial pressure of O2 in lungs,
hemoglobin becomes practically saturated with O2.
d. At the O2 partial pressures in the tissues,
oxyhemoglobin quickly unloads much of its O2.
e. The acid pH and warmer temperature of the tissues
also promote this dissociation.
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Loading and Unloading Reactions
In the lungs: loading reaction
Deoxy-Hb + O2  oxy-Hb;
In tissues (unloading reaction) occurs.
Oxy-Hb  Deoxy-Hb + O2
Loading/unloading reactions are affected by: PO2 and Hb
affinity to O2.
In the lungs, the oxy-Hb saturation is 97% (20 ml O2 /100
ml blood). This is reduced to 75% (15.5 ml O2 /100 ml)
in blood leaving tissues.
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CO2 Transport
Carbon dioxide transport:
 ~9% dissolved in plasma
 ~13% attached to Hb as carbaminohemoglobin
 ~78% converted to bicarbonate ion HC03- CO2 + H2O  H2CO3  H+ + HCO3-
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Body tissue
CO2 produced
CO2 transport
from tissues
Interstitial
CO2
fluid
Plasma
CO2
within capillary
Capillary
wall
CO2
H2O
Red
blood
cell
H2CO3
Hb
Carbonic
acid
HCO3 
Bicarbonate
Hemoglobin (Hb)
picks up
CO2 and H+.
H+
HCO3
To lungs
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To lungs
CO2 transport
to lungs
HCO3
HCO3 
H2CO3
H+
Hb
Hemoglobin
releases
CO2 and H+.
H2O
CO2
CO2
CO2
CO2
Alveolar space in lung